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HEPATORENAL FAILURE - 05/09/11

Doi : 10.1016/S1089-3261(05)70102-1 
Florence Wong, MD a, Laurence Blendis, MD a, b
a Division of Gastroenterology, Department of Medicine, University of Toronto, Toronto, Ontario, Canada (FW, LB) 
b Institute of Gastroenterology, Ichilov Hospital, Tel Aviv, Israel (LB) 

Résumé

Progressive oliguric renal failure is a common and severe complication seen in patients with advanced liver disease, especially in patients with cirrhosis and ascites. More than 100 years ago, Austin Flint35 noted that patients with advanced cirrhosis and ascites developed oliguria as a preterminal event. He commented on the dismal outcome of various therapeutic options, “[W]e may make cautious trial of diuretics and hydragogue cathartics. If these means do not prove promptly efficacious (as they will rarely do), it is useless to persist in the former (diuretics) and injurious to consider the latter (hydragogues).” He further commented that of the 11 patients whose autopsied kidneys were available, 5 were considered to be normal, and the remaining 6 were diseased. Thus, it was already recognized that both functional and structural renal diseases could occur in patients with advanced liver disease.

The combination of acute liver failure and renal failure can occur as a result of conditions that directly involve both the liver and the kidney or in conditions where the primary disorder is in the liver with secondary renal involvement. Simultaneous renal and liver damage can result from involvement of both organs in systemic conditions, including collagen vascular diseases, infiltrative disorders such as amyloidosis, and congenital disorders such as polycystic disease, acute fatty liver, or toxemia of pregnancy. Exposure to toxins, such as acetaminophen overdose, is frequently associated with both liver and renal failure. The fluorinated anesthetic agents methoxyfluorane and fluroxene can cause both hepatic and renal damage. Derangement of renal function secondarily complicating primary disorders of the liver are much more common, however. Intrinsic renal disorders, in which there is structural renal damage are seen with several liver diseases. For example, IgA nephropathy is peculiar to alcoholic liver disease, but is not seen in other liver conditions. Glomerulonephritis may be associated with hepatitis B and hepatitis C infection. Renal tubular acidosis, a syndrome associated with failure of the kidney to acidify the urine, can occur in either alcoholic cirrhosis or autoimmune hepatitis. Table 1 lists some of the renal abnormalities associated with liver diseases.

In contrast, functional renal disease occurs much more frequently in patients with advanced cirrhosis, especially in those patients with ascites. The term hepatorenal syndrome (HRS), which denotes the most severe form of functional renal disorder, was first coined about 60 years ago to describe acute renal failure following biliary surgery.55 The definition of HRS has gradually evolved. In 1956, Sherlock noted that the renal failure observed in patients with the terminal stages of cirrhosis was associated with a low urinary sodium and an absence of proteinuria.53 In 1958, Papper and his colleagues98 were the first to suggest that the pathogenesis of HRS was related to circulatory disturbance of an otherwise normal kidney. These findings were confirmed by Vesin132 and by Baldus and associates,10 who emphasized the functional nature of HRS. During the last three decades, it has become clear that the circulatory disturbance of chronic liver disease is the basis of many of the major complications, stimulating much research into its pathogenesis to improve treatment options.

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 Address reprint requests to Laurence Blendis, MD, Division of Gastroenterology, Department of Medicine, 9EN/220 Toronto General Hospital, 200 Elizabeth Street, Toronto M5G 2C4, Ontario, Canada


© 2000  W. B. Saunders Company. Publié par Elsevier Masson SAS. Tous droits réservés.© 1993 
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Vol 4 - N° 1

P. 169-189 - février 2000 Retour au numéro
Article précédent Article précédent
  • ASCITES
  • Telfer B. Reynolds
| Article suivant Article suivant
  • PEDIATRIC HEPATOLOGY : A Half-Century of Progress
  • William F. Balistreri

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